Short-term improvement of endothelial function in rituximab-treated rheumatoid arthritis patients refractory to tumor necrosis factor α blocker therapy




Cardiovascular disease is the major cause of excessive mortality in rheumatoid arthritis (RA) and endothelial dysfunction plays a key role in atherosclerosis. The aim of the present study was to assess whether rituximab therapy was able to improve endothelial function in RA patients refractory to tumor necrosis factor α (TNFα) blockers.


Six consecutive RA patients (5 women; age range 55–79 years) with active disease refractory to TNFα inhibitor therapy were studied. Patients received intravenous rituximab (1 course, consisting of 2 infusions of 1,000 mg each separated by 2 weeks). Flow-mediated endothelium-dependent vasodilatation (FMD%) and endothelium-independent vasodilatation (postnitroglycerin) were measured at day 0 prior to the first rituximab infusion, at week 2 (before the second infusion), and at month 6.


At week 2, a dramatic increase in FMD% values was observed in all patients (mean ± SD 7.02 ± 2.31%, median 7.29%, range 3.2–9.75%) compared with those observed before the first infusion (mean ± SD 3.35 ± 1.58%, median 3.04%, range 1.69–5.89%). In addition, at month 6, FMD% values in all patients (mean ± SD 7.66 ± 1.73%, median 7.64%, range 5.61–9.98%) were greater than those found before the first infusion (P = 0.03). The dramatic improvement of FMD% was associated with a significant decrease in C-reactive protein level and Disease Activity Score in 28 joints.


Our study demonstrates an active effect of rituximab on endothelial function in RA patients refractory to TNFα blockers.